Regional Transport

Question 1

Impact of cathecolamines and angiotensin II on Na reabsorption

Answer 1

⬆️ fraction of Na reabsorbed in PT

*(+) baso lateral Na/K ATPase

Question 2

How is the absorption of HCO3 in a volume depleted state? Why?

Answer 2

• ⬆️ HCO3 reabsorption in PT

- ⬆️ Ag II (+) Na-H antiporter

Question 3

Principal factor that control H+ secretion from PT cell and thus HCO3 reabsorption. How are they at acidosis and alkalosis state?

Answer 3

• [H+] in the cell

- ⬆️ both in acidosis and ⬇️ both in alkalosis

Question 4

What would happen if you block carbonic anhydrase (azetazolamide) in PT? What condition could result?

Answer 4

• ⬇️ HCO3 reabsorption and activity of Na-H antiporter

- type II Renal Tubular Acidosis

Question 5

Common causes of contraction alkalosis (metabolic alkalosis). Mechanism of production of it.

Answer 5

• low volume state: sweating in desert, vomiting, thiazide diuretic
• ⬆️ Ag II ▶️ ⬆️ HCO3 reabsorption

Question 6

Why diarrhea doesn’t cause contraction alkalosis, although it promotes a low volume state?

Answer 6

Lose HCO3 in stools ▶️ metabolic acidosis

Question 7

Why in Fanconi syndrome the chloride doesn’t follow the loss of Na, K and H2O? How is the complete metabolic condition?

Answer 7

• curiously the Cl reabsorption ⬆️ ▶️ maintain neutrality ▶️ no anion gap
• metabolic acidosis hypokalemic hyperchloremic

Question 8

Why does the inulin concentration increase along the nephron? Where is the lower and higher inulin concentration?

Answer 8

• 2/3 water reabsorption in PT ▶️ [inulin] triple, continue ⬆️ in rest tubule system (assuming ADH acts)
• lower: bowman’s space, higher: terminal collecting duct

Question 9

Function of the descending limb of loop of henle

Answer 9

Reabsorb 15% of filtered water

Question 10

Treatment of hyponatremia, low serum osmolality and high urine osmolality in SIADH

Answer 10

• fluid restriction
• loop diuretic ▶️ ⬆️ plasma Na

*loop diuretic ▶️ ⬇️ reabsorption of NaCl at loop of henle ▶️ remove the concentrating function of it ▶️ ⬇️ osmolar gradient ▶️ ⬇️ reabsorption of free water from collecting duct (“fluid restriction like”)

Question 11

Why Bartter’s syndrome leads secondary hiperaldosteronism? Some features of it.

Answer 11

• Presents a low volume state ▶️ ⬆️ renin and aldosterone
• hypokalemia, high urine Ca (low positive luminal potential), alkalosis

*genetic mutation of Na/K/2Cl transporter of loop of henle ▶️ dysfunction

Question 12

Cause of familial hypocalciuric hypercalcemia (FHH)

Answer 12

Calcium-sensing receptor (CaSR) autosomal dominant mutation

*as also present in parathyroid gland ▶️ ⬆️ PTH (not sense ⬆️ Ca)

Question 13

What is Gitelman’s syndrome and some of its features

Answer 13

• mutation (dysfunction) NaCl transporter of distal tubule

- hyookalemia, alkalosis, low urine Ca (difference with alteration of Na-K-2Cl transporter of loop of henle)

Question 14

Acid-base disturbance in case of excess of Aldosterone

Answer 14

Metabolic alkalosis

Question 15

How can the potassium sparing diuretics work?

Answer 15

• block ENac (amiloride)
• block aldosterone receptor (spironolactone)
• block production aldosterone (RAAS system blocker)

*more specific: splerenone (less side effects)

Question 16

What is cause of the Liddle’s syndrome? and some of their features. How do you treat it?

Answer 16

• mutation ▶️ gain function ENac in CD ▶️ ⬆️ Na reabsorption and K secretion
• HTN, hyookalemia, metabolic alkalosis.
• amiloride

Question 17

What segments of the tubule system reabsorbs HCO3?

Answer 17

• proximal tubules (80% filtered)
• ascending limb of loop of henle

*both Na-H antiporter and carbonic anhydrase need to it

Question 18

Why does a high aldosterone state (hyperaldosteronism) results in metabolic alkalosis and hypokalemia?

Answer 18

• ⬆️ secretion of H (by H-ATPase) ▶️ ⬆️ production HCO3
• ⬆️ secretion K because ⬆️ reabsorption Na (by ENaC)

*ex: Conn syndrome (primary hyperaldosteronism)

Question 19

What type of renal tubular acidosis leads in hyperkalemia? Why? Causes

Answer 19

• type IV: hypoaldosterone state
• inability to secrete K and H
• diabetic nephropathy (⬇️ renin), AECI, ARBs, spironolactone, aliskiren, Trimetoprim, Addison disease (loss aldosterone secretion from adrenal cortex)

Question 20

Why insulin and epinephrine can reduce plasma potassium?

Answer 20

(+) Na/K ATPase

Question 21

In what case when there is a metabolic acidosis, can be present a hypokalemia? (Remember classically acidosis leads hyperkalemia)

Answer 21

• diarrhea

* loss of HCO3 in stool ▶️ metabolic acidosis hiperchloremic with hypokalemia